Inmostformsofartificialrespiration(mouth-to-mouthresuscitation,mechanicalrespiration),endotrachealpressureaboveatmosphericpressureisusedtoinflatethelungs,andexpirationoccursbypassiverecoilofthethoraciccage(see ).Thuslunginflationisaccompaniedbyanappreciableriseinintrathoracicpressure.Venacavalflowdecreasessharplyduringthephaseofpositive-pressurelunginflationwhentheendotrachealpressureprogressivelyrises.Whennegativeendotrachealpressureisusedtofacilitatedeflation,venacavalflowacceleratesmorethanwhenthelungsareallowedtodeflatepassively.
Sustained expiratory efforts increase intrathoracic pressure and thus impede venous return. Straining against a closed glottis (Valsalva’s maneuver) regularly occurs during coughing, defecation, and heavy lifting. Intrathoracic pressures in excess of 100 mm Hg have been recorded in trumpet players, and pressures higher than 400 mm Hg have been observed during paroxysms of coughing. Such increases in pressure are transmitted directly to the lumens of the intrathoracic arteries. After coughing stops, arterial blood pressure may fall precipitously because of the preceding impediment to venous return.
Interplay of Central and Peripheral Factors in Control of the Circulation
The primary function of the circulatory system is to deliver the nutrients needed for tissue metabolism and growth and to remove the products of metabolism. The contributions of the components of the cardiovascular system to maintain adequate tissue perfusion under different physiological conditions were discussed previously. In this section, the interrelationships among the various components of the circulatory system are explored. The autonomic nervous system and the baroreceptors and chemoreceptors play key roles in regulating the cardiovascular system. Control of fluid balance by the kidneys, with maintenance of a constant blood volume, is also very important.
In any well-regulated system, one way to evaluate the extent and sensitivity of its regulatory mechanisms is to disturb the system and to observe how it restores the preexisting steady state. Two such disturbances, physical exercise and hemorrhage, are discussed in the following sections to illustrate operation of the various regulatory factors.
The cardiovascular adjustments that occur during exercise consist of a combination of neural and local (chemical) factors. Neural factors include (1) central command, (2) reflexes that originate in the contracting muscle, and (3) the baroreceptor reflex. Central command is the cerebrocortical activation of the sympathetic nervous system that produces cardiac acceleration, increased myocardial contractile force, and peripheral vasoconstriction. Reflexes are activated intramuscularly by stimulation of mechanoreceptors (by stretch, tension) and chemoreceptors (by metabolic products) in response to muscle contraction. Impulses from these receptors travel centrally via small myelinated (group III) and unmyelinated (group IV) afferent nerve fibers. Group IV unmyelinated fibers may represent the muscle chemoreceptors, inasmuch as no morphological chemoreceptor has been identified. The central connections of this reflex are unknown, but the efferent limb consists of sympathetic nerve fibers to the heart and peripheral blood vessels. The baroreceptor reflex is described in , and local factors that influence skeletal muscle blood flow (metabolic vasodilators) are described in . Vascular chemoreceptors are important in regulation of the cardiovascular system during exercise. Evidence for this assertion comes from the observations that the PaCO2, the PaO2, and the pH of arterial blood remain normal during exercise.
Mild to Moderate Exercise
In humans or trained animals, anticipation of physical activity inhibits vagal nerve impulses to the heart and increases sympathetic discharge. The result is an increase in heart rate and myocardial contractility. The tachycardia and enhanced contractility increase cardiac output.